The "Hard" Science of Depression

Depression is a word we have begun to hear quite frequently in our lives.  Friends claiming to have had a "depressing" day, a book or movie was particularly "depressing", and of course the all too common, "I just feel depressed."  With all of this talk about depression one seems to lose the value of what clinical depression truly means and what it really is.  What talks like Dr. Silton's talk and other ongoing research are helping to do is establish an acceptable, understandable, and dependable definition for what depression REALLY is.

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First it is helpful to define depression as the way it is currently defined under the DSM.  It is categorically defined, meaning you are either depressed or not depressed, and diagnosis under the DSM requires "two or more major depressive episodes... depressed mood and/or loss of interest or pleasure in life activities for at least 2 weeks..." and at least five of nine symptoms from criteria created by the DSM (http://www.ncbi.nlm.nih.gov/books/NBK64063/).  This definition, though fairly descriptive of the mood and its effects, is lacking a few key aspects of what is now used to characterize and treat illnesses, which include: biological, physiological, and genetic causes.  Dr. Silton's talk brought to light some research that she and others have done and continue to do that are showing these "hard science" evidences do exist in the case of depression.  This evidence may be showcased best in a study done by Caspi et al. in 2003.

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This study focused on how stressful life events influence depression but with the moderation of the serotonin transporter (5-HTT) gene.  This gene can be homozygous long (l/l), homozygous short (s/s), or heterozygous (s/l).  For the study a birth cohort of 1037 children were assessed at the ages of 3, 5, 7, 9, 11, 13, 15, 18, and 21.  This group was split into three subgroups, those with the l/l genotype, the s/l genotype, and the s/s genotype.   Eventually stressful life events between the ages of 21 and 26 were measured using the life-history calendar method.  These included multiple categories including: employment, finance, housing, health, and relationship stressors.  What the study found was that those who had the s/s genotype had higher self reported depression symptoms, higher probabilities of suicide ideation and major depressive episodes, and higher informant reports of depression as the number of stressful life events increased.  What this shows, and what the authors of the paper argue, is that there is a gene and environment interaction (Caspi et al. 2003).

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What this article shows is that both environmental factors and biological/physiological factors are important and must be researched further to better define and treat depression in the future.  This type of mission has been started for all psychiatric disorders in the form of RDoC (Research Domain of Criteria).  RDoC's mission is to create "new ways of classifying psychopathology based on dimension of observable behavior and neurobiological measures" (http://www.nimh.nih.gov/research-priorities/rdoc/index.shtml).  The undertaking of this kind of project is a great step for all of mental health.  Both Dr. Silton's talk and the paper written by Caspi and other researchers exemplifies the steps we, as those interested in the field of neuroscience, can and must take to advance the understanding and treatments of mental illnesses.  With the rapid growth in technologies and in our knowledge of the brain there is no reason we cannot expand and improve upon this already great research being done in the field.